scholarly journals NF-κB suppresses apoptosis and promotes bladder cancer cell proliferation by upregulating survivin expression in vitro and in vivo

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Xiaolu Cui ◽  
Dezhi Shen ◽  
Chuize Kong ◽  
Zhe Zhang ◽  
Yu Zeng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Survivin Expression ◽  
Bladder Cancer Cell ◽  
Cancer Cell Proliferation

scholarly journals Effects of agents that inhibit cellular iron incorporation on bladder cancer cell proliferation

Blood ◽  
1993 ◽  
Vol 82 (5) ◽  
pp. 1608-1617 ◽  
Author(s):  
PA Seligman ◽  
RB Schleicher ◽  
G Siriwardana ◽  
J Domenico ◽  
EW Gelfand
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Cellular Proliferation ◽  
Bladder Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Inhibition Of Proliferation ◽  
Cellular Iron

Abstract Agents that interfere with cellular iron (Fe) incorporation inhibit tumor cell proliferation, including metals that bind to transferrin (Tf) such as gallium (Ga) or indium (In) and Fe chelators such as desferrioxamine (DFO). Ga nitrate is effective in the treatment of metastatic bladder cancer and these patients exhibit evidence for interference with Fe metabolism. We show here that bladder cancer cell proliferation in vitro is dependent on Tf-Fe. Concentrations of DFO that can be readily achieved in vivo inhibit cellular proliferation even in the presence of physiologic concentrations of Tf-Fe. Inhibition of proliferation by Tf-Ga is associated with decreased cellular Fe incorporation. However, when a physiologic concentration of Tf-Fe is added to an equimolar concentration of Tf-Ga, significant Fe incorporation is evident despite inhibition of proliferation. Thus, besides interference with Fe incorporation, Ga may also interfere with intracellular Fe distribution and/or directly inhibit an Fe- (or non-Fe- ) requiring process necessary for cellular proliferation. DFO followed sequentially by Tf-Ga results in marked potentiation of inhibition of proliferation. The effects of this combination appear to be related to both interference with Fe metabolism and increased Ga uptake. This sequential combination may be useful in the treatment of bladder cancer.

scholarly journals Effects of agents that inhibit cellular iron incorporation on bladder cancer cell proliferation

Blood ◽  
1993 ◽  
Vol 82 (5) ◽  
pp. 1608-1617 ◽  
Author(s):  
PA Seligman ◽  
RB Schleicher ◽  
G Siriwardana ◽  
J Domenico ◽  
EW Gelfand
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Cellular Proliferation ◽  
Bladder Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Inhibition Of Proliferation ◽  
Cellular Iron

Agents that interfere with cellular iron (Fe) incorporation inhibit tumor cell proliferation, including metals that bind to transferrin (Tf) such as gallium (Ga) or indium (In) and Fe chelators such as desferrioxamine (DFO). Ga nitrate is effective in the treatment of metastatic bladder cancer and these patients exhibit evidence for interference with Fe metabolism. We show here that bladder cancer cell proliferation in vitro is dependent on Tf-Fe. Concentrations of DFO that can be readily achieved in vivo inhibit cellular proliferation even in the presence of physiologic concentrations of Tf-Fe. Inhibition of proliferation by Tf-Ga is associated with decreased cellular Fe incorporation. However, when a physiologic concentration of Tf-Fe is added to an equimolar concentration of Tf-Ga, significant Fe incorporation is evident despite inhibition of proliferation. Thus, besides interference with Fe incorporation, Ga may also interfere with intracellular Fe distribution and/or directly inhibit an Fe- (or non-Fe- ) requiring process necessary for cellular proliferation. DFO followed sequentially by Tf-Ga results in marked potentiation of inhibition of proliferation. The effects of this combination appear to be related to both interference with Fe metabolism and increased Ga uptake. This sequential combination may be useful in the treatment of bladder cancer.

scholarly journals The lncRNA DLX6-AS1 promoted cell proliferation, invasion, migration and epithelial-to-mesenchymal transition in bladder cancer via modulating Wnt/β-catenin signaling pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jinan Guo ◽  
Zhixin Chen ◽  
Hongtao Jiang ◽  
Zhou Yu ◽  
Junming Peng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Bladder Cancer Cell ◽  
Mesenchymal Transition ◽  
Bladder Cancer Cells

Abstract Background Bladder cancer is the most common human urological malignancies with poor prognosis, and the pathophysiology of bladder cancer involves multi-linkages of regulatory networks in the bladder cancer cells. Recently, the long noncoding RNAs (lncRNAs) have been extensively studied for their role on bladder cancer progression. In this study, we evaluated the expression of DLX6 Antisense RNA 1 (DLX6-AS1) in the cancerous bladder tissues and studied the possible mechanisms of DLX6-AS1 in regulating bladder cancer progression. Methods Gene expression was determined by qRT-PCR; protein expression levels were evaluated by western blot assay; in vitro functional assays were used to determine cell proliferation, invasion and migration; nude mice were used to establish the tumor xenograft model. Results Our results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis. The in vitro experimental data showed that DLX6-AS1 overexpression promoted bladder cancer cell growth, proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT); while DLX6-AS1 inhibition exerted tumor suppressive actions on bladder cancer cells. Further results showed that DLX6-AS1 overexpression increased the activity of Wnt/β-catenin signaling, and the oncogenic role of DLX6-AS1 in bladder cancer cells was abolished by the presence of XAV939. On the other hand, DLX6-AS1 knockdown suppressed the activity of Wnt/β-catenin signaling, and the tumor-suppressive effects of DLX6-AS1 knockdown partially attenuated by lithium chloride and SB-216763 pretreatment. The in vivo tumor growth study showed that DLX6-AS1 knockdown suppressed tumor growth of T24 cells and suppressed EMT and Wnt/β-catenin signaling in the tumor tissues. Conclusion Collectively, the present study for the first time identified the up-regulation of DLX6-AS1 in clinical bladder cancer tissues and in bladder cancer cell lines. The results from in vitro and in vivo assays implied that DLX6-AS1 exerted enhanced effects on bladder cancer cell proliferation, invasion and migration partly via modulating EMT and the activity of Wnt/β-catenin signaling pathway.

scholarly journals Testicular Nuclear Receptor 4 Regulates Proliferation and Apoptosis of Bladder Cancer via Bcl-2

2021 ◽  
Vol 8 ◽  
Author(s):  
Huan Wang ◽  
Wenqin Luo ◽  
Xuliang Wang ◽  
Dingwei Xue ◽  
Liangliang Ren ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Nuclear Receptor ◽  
Cancer Cell ◽  
Nuclear Hormone Receptor ◽  
Bladder Cancer Cell ◽  
Control Group ◽  
Lower Grade ◽  
Cancer Cell Proliferation

Testicular nuclear receptor 4 (TR4) is a member of the nuclear hormone receptor family and acts as a ligand-activated transcription factor and functions in many biological processes, such as development, cellular differentiation, and homeostasis. Recent studies have shown that TR4 plays an important role in prostate cancer, renal cell carcinoma, and hepatocellular carcinoma; however, its potential link to bladder cancer (BC) remains unknown. This study found that bladder cancer exhibited a higher expression of TR4 compared to normal tissues. Overexpressed TR4 promoted the bladder cancer cell proliferation, and knocked down TR4 with TR4-siRNA suppressed the bladder cancer cell proliferation. Mechanistic studies reveal that TR4 functions by altering the expression of Bcl-2 to regulate apoptosis in bladder cancer cells. Furthermore, knocking down Bcl-2 reversed the BC proliferation induced by TR4. In vivo, we also confirmed that TR4 knockdown mice (TR4+/−) showed slower bladder cancer growth than wild-type mice (TR4+/+) induced by the carcinogenic chemicals. Moreover, TR4+/− mice showed a lower grade of histopathology than the control group. In conclusion, these results indicate that TR4 plays a key role in bladder cancer proliferation, and targeting TR4 would probably be a potential strategy for bladder cancer treatment.

scholarly journals Semaphorin 4D promotes the proliferation and metastasis of bladder cancer by activating the PI3K/AKT pathway

2019 ◽  
Vol 105 (3) ◽  
pp. 231-242 ◽  
Author(s):  
Jian-jun Lu ◽  
Yao-wu Su ◽  
Chao-jun Wang ◽  
Di-feng Li ◽  
Liang Zhou
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Akt Pathway ◽  
Semaphorin 4D ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

The present study aimed to investigate the role of semaphorin 4D (Sema4D) in bladder cancer cell proliferation and metastasis in vivo and in vitro. Effects of Sema4D modulation on cancer cell viability and clonogenic abilities were assessed by MTT assay and colony formation assay. Cell apoptosis, cell cycle analysis, transwell assays, and wound-healing assays were also assayed. A mouse model of bladder cancer was established to observe the tumorigenesis in vivo. Our data showed that Sema4D was 4-fold upregulated in clinical bladder cancer tissues relative to noncancerous ones and differentially expressed in bladder cancer cell lines. Knockdown of Sema4D in bladder cancer T24 and 5637 cells significantly decreased cell proliferation, clonogenic potential, and motility. On the contrary, overexpression of Sema4D in bladder cancer SV-HUC-1 cells significantly increased cell viability and motility. Concordantly, knockdown of Sema4D impaired while overexpression of Sema4D promoted bladder cancer cell growth rates in xenotransplanted mice. Cell cycle was arrested by modulation of Sema4D. Cell apoptotic rates and the mitochondrial membrane potentials were consistently increased upon knockdown of Sema4D in T24 cells and 5637 cells. Western blotting revealed that epithelial–mesenchymal transition was promoted by Sema4D. The PI3K/AKT pathway was activated upon Sema4D overexpression in SV-HUC-1 cells, while it was inactivated by knockdown of Sema4D in T24 cells. All these data suggest that Sema4D promotes cell proliferation and metastasis in bladder cancer in vivo and in vitro. The oncogenic behavior of Sema4D is achieved by activating the PI3K/AKT pathway.

scholarly journals THE IMPACT OF MORPHINE TREATMENT ON BLADDER CANCER CELL PROLIFERATION AND APOPTOSIS: IN VITRO STUDIES

2018 ◽  
Vol 40 (3) ◽  
pp. 190-193 ◽  
Author(s):  
P Harper ◽  
O Hald ◽  
B A Lwaleed ◽  
A Kyyaly ◽  
D Johnston ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Western Blot ◽  
Opioid Receptor ◽  
Cancer Cell ◽  
Receptor Expression ◽  
Bladder Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Proliferation And Apoptosis

Aim: The aim of this study was to determine the effect of morphine on bladder cancer cell proliferation and apoptosis in vitro. Materials and Methods: MTT assay was used to measure percentage growth of RT-112 human bladder cancer cells after 72 hours of morphine/morphine + naloxone treatment. Expression of µ-opioid receptors was assessed by Western blot and finally, apoptotic assay with CellEvent Caspase-3/7 Green Detection Reagent was carried out using confocal microscopy. Results: The MTT assays showed that morphine increased RT-112 cell growth. Naloxone inhibited this growth enhancing effect. Western blot analysis regarding µ-opioid receptor expression in RT-112 cells remains inconclusive. Morphine was also found to decrease the rate of apoptosis of RT-112 cells, an effect which naloxone inhibited. Conclusions: This study provides evidence that morphine, at clinically relevant doses, causes RT-112 bladder cancer cell proliferation, possibly opioid receptor mediated and at least some of this effect might be due to decreased apoptosis. Clinically, this suggests that in patients with bladder cancer, managing pain with morphine might have detrimental consequences on patient outcomes and alternative pain relief should be considered if possible.

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